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@ARTICLE{Wortmann:130974,
      author       = {M. Wortmann and M. Hakimi and T. Fleming and A. S. Peters
                      and T. Sijmonsma$^*$ and S. Herzig$^*$ and P. P. Nawroth and
                      D. Böckler and S. Dihlmann},
      title        = {{A} {G}lyoxalase-1 {K}nockdown {D}oes {N}ot {H}ave {M}ajor
                      {S}hort {T}erm {E}ffects on {E}nergy {E}xpenditure and
                      {A}therosclerosis in {M}ice.},
      journal      = {Journal of diabetes research},
      volume       = {2016},
      issn         = {2314-6753},
      address      = {New York, NY [u.a.]},
      publisher    = {Hindawi},
      reportid     = {DKFZ-2017-06050},
      pages        = {1 - 8},
      year         = {2016},
      abstract     = {Objective. Glyoxalase-1 is an enzyme detoxifying
                      methylglyoxal (MG). MG is a potent precursor of advanced
                      glycation endproducts which are regarded to be a key player
                      in micro- and macrovascular damage. Yet, the role of Glo1 in
                      atherosclerosis remains unclear. In this study, the effect
                      of Glo1 on mouse metabolism and atherosclerosis is
                      evaluated. Methods. Glo1 knockdown mice were fed a high fat
                      or a standard diet for 10 weeks. Body weight and composition
                      were investigated by Echo MRI. The PhenoMaster system was
                      used to measure the energy expenditure. To evaluate the
                      impact of Glo1 on atherosclerosis, Glo1(KD) mice were
                      crossed with ApoE-knockout mice and fed a high fat diet for
                      14 weeks. Results. Glo1 activity was significantly reduced
                      in heart, liver, and kidney lysates derived from Glo1(KD)
                      mice. Yet, there was no increase in methylglyoxal-derived
                      AGEs in all organs analyzed. The Glo1 knockdown did not
                      affect body weight or body composition. Metabolic studies
                      via indirect calorimetry did not show significant effects on
                      energy expenditure. Glo1(KD) mice crossed to ApoE(-/-) mice
                      did not show enhanced formation of atherosclerosis.
                      Conclusion. A Glo1 knockdown does not have major short term
                      effects on the energy expenditure or the formation of
                      atherosclerotic plaques.},
      keywords     = {Apolipoproteins E (NLM Chemicals) / Pyruvaldehyde (NLM
                      Chemicals) / Lactoylglutathione Lyase (NLM Chemicals)},
      cin          = {A170},
      ddc          = {610},
      cid          = {I:(DE-He78)A170-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26788517},
      pmc          = {pmc:PMC4693023},
      doi          = {10.1155/2016/2981639},
      url          = {https://inrepo02.dkfz.de/record/130974},
}